Oxygen-effect as an inhibition of repair: radiation studies on excision repair deficient mei-9L1-embryos of Drosophila.
The excision repair deficient mei-9L1-embryos of Drosophila melanogaster are up to four times more radiosensitive than normal +/+ embryos. The lack of oxygen-effect in the repair deficient 4-h-embryos and the reduced O2-effect in the 13/4-h embryos suggest an interpretation of the oxygen effect as a modification of the ability to repair. The conversion of the early death (heavy damage) to late death (slight damage) by irradiation of normal embryos in N2 supports this interpretation. This theory can also explain the dependence of O2-effect on LET. The spontaneous lethality and the increase in radiosensitivity depend in heterozygous mei-9L1-embryos strictly upon the genotype of the mother, thus representing a maternal effect.
D000818:Animals; D004307:Dose-Response Relationship, Radiation; D004331:Drosophila melanogaster / Q000196:embryology* / Q000235:genetics / Q000528:radiation effects; D004735:Energy Transfer; D009026:Mortality; D009154:Mutation; D010100:Oxygen / Q000494:pharmacology*; D011836:Radiation Tolerance
D010100:Oxygen